The precise mechanism of the anti-tumor effect of imiquimod in BCC is not known. It has been postulated that ultraviolet radiation induces mutations in the tumor-suppressor genes and alters the immuno-surveillance, so that tumor cells escape from cytotoxic T cells and apoptosis.[1] Th-2 cytokines, that downregulate tumor surveillance, are raised in BCC.[1],[5] Imiquimod acts on toll-like receptor-7 (TLR-7) present on dendritic cells, macrophages and monocytes and induces expression of interferons, Th-1 cytokines (IL-1, IL-6, IL-10 and IL-12), tumor necrosis factor-a and G-CSF, thereby counteracting Th2 cytokines and promoting tumor surveillance.[1],[5] It also enhances the activity of natural killer cells and epidermal Langerhans' cells. The tumor regression is achieved probably by induction of Fas receptors on the tumor cells resulting in their apoptosis.[10]

Clinical clearance rate at 1, 2 and 3 years were 94, 76 and 70%, respectively. We conclude that imiquimod seems to be an appropriate therapeutic alternative for the treatment of recurrent BCC in patients with associated co-morbidities.

The proportion of subjects who were clinically clear at the 2-year follow-up visit was estimated to be 82.0%. Imiquimod was tolerated when applied daily, with erythema reported for all subjects participating in the study. The recurrence rate observed suggests that once daily dosing and 5x/week dosing yield similar clearance rates, but daily dosing increases local skin reactions.

Raasch B. Clinical, Cosmetic and Investigational Dermatology. 9 June 2009. There is reasonable evidence that the use of imiquimod for small (<2 cm) superficial BCC that occur other than on the face provides outcomes only marginally less satisfactory t

There is reasonable evidence that the use of imiquimod for small (<2 cm) superficial BCC that occur other than on the face provides outcomes only marginally less satisfactory than surgery. There would be a place for imiquimod in treating patients with frequent multiple primary lesions when access to surgery is difficult or where clinical judgment may be influenced by patient factors as reported in some of the studies, eg, where patients may have contraindications to surgery. It was noted that if recurrences occurred in this study they mostly occurred during the first 9 months after the end of treatment. The initial response was therefore predictive of long-term outcome so these authors recommend and encourage continued monitoring of skin lesions.

To date one long-term study indicates a treatment success rate of 78%-81% and that initial response is a predictor of long-term outcome. Recurrences tend to occur within the first year after treatment. Future research will compare this preparation to the gold standard treatment for superficial BCC - surgical excision.

Composite clearance rates (combined clinical and histological assessments) for the 5 and 7x/week imiquimod groups were 75% and 73%, respectively. Histological clearance rates for the 5 and 7x/week imiquimod groups were 82% and 79%, respectively. Increasing severity of erythema, erosion, and scabbing/crusting was associated with higher clearance rates. CONCLUSION: Imiquimod appears to be safe and effective for the treatment of sBCC when compared with vehicle cream. The difference in clearance rates between the two imiquimod dosing groups was not significant. The 5x/week regimen is recommended.

For patients without comorbidities, the overall cure rate was 73%. For these patients, the cure rates were 85.7% for superficial and nodular BCC, 88% for superficial BCC, 57% for Bowen's disease, 50% for nodular BCC, and 50% for aggressive BCC.